Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA287787 | ENA |
REPOSITORIES: ENA
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Project description:The deafness gene DFNA5 induces programmed cell death through mitochondria and MAPK-related pathways [HEK293T]
| PRJNA287787 | ENA
Project description:The deafness gene DFNA5 induces programmed cell death through mitochondria and MAPK-related pathways
| PRJNA287784 | ENA
Project description:The deafness gene DFNA5 induces programmed cell death through mitochondria and MAPK-related pathways [BY4741]
| PRJNA287786 | ENA
Project description:In this study, we investigated how nicotinamide (NAM) affects cellular metabolism in TNBC cells and also such altered cellular metabolism by NAM is linked to cytotoxic functions through an integrated analysis of proteome and transcriptome data generated from three different TNBC cell lines, BT20, MB468, and MB231. By analyzing mRNA-seq data from control and NAM treated TNBC cells (3 replicates in each of 3 cell lines), we identified differentially expressed genes (DEGs), and associated cellular process. The up-regulated genes were associated with the processes related to cell death (programmed cell death, autophagy, and apoptotic mitochondrial changes) and mitochondria (organization, pH reduction/oxidation-reduction/NADP metabolism, response to starvation, respiratory chain, and lipid/oxoacid metabolism). On the other hand, the processes related to immune response (NF-kB and MAPK signaling, cell adhesion/migration, and response to cytokine) and cell proliferation were down-regulated consistently in the three TNBC cells.
2021-04-22 | GSE172494 | GEO
Project description:The function of DFNA5 remained unknown for a long time, but previous functional studies by Op de Beeck et al. (2011) revealed that DFNA5 induces a growth defect in mutDFNA5- transfected HEK293T cells, as well as other cells, leading to PCD (Op de Beeck et al., 2011). The cell death-inducing capacity of DFNA5 was not only restricted to human cell lines, but was also observed in the yeast model Saccharomyces cerevisiae (Van Rossom et al., 2012). This inspired us to perform a transcriptomic analysis using two different model organisms (mammalian, HEK293T, and yeast, S.cerevisiae) to further elucidate the mechanisms related to DFNA5. Comparison of 2 transfected yeast cell populations in 2 different growth phases. In total, 4 comparisons were made, each comparison was done in duplo by a colourflip. Every conditions is represented through 2 biol reps.
2015-06-24 | E-GEOD-70168 | biostudies-arrayexpress
Project description:This model is from the article:
Systems biology analysis of programmed cell death
Shani Bialik, Einat Zalckvar, Yaara Ber, Assaf D. Rubinstein, Adi Kimchi Trends in Biochemical Sciences
Volume 35, Issue 10, 556-564, 27 May 2010 20537543
,
Abstract:
Systems biology, a combined computational and experimental approach to analyzing complex biological systems, has recently been applied to understanding the pathways that regulate programmed cell death. This approach has become especially crucial because recent advances have resulted in an expanded view of the network, to include not just a single death module (apoptosis) but multiple death programs, including programmed necrosis and autophagic cell death. Current research directions in the systems biology field range from quantitative analysis of subprocesses of individual death pathways to the study of interconnectivity among the various death modules of the larger network. These initial studies have provided great advances in our understanding of programmed cell death and have important clinical implications for drug target research.
Brief Note about the model:
This model is an export of 26 SPIKE
Apoptosis Networks to SBML format.
This is a pathway model (not quantitative model) of Apoptosis.
Apoptosis, or type I cell death, is a form of programmed cell death
characterized by fragmentation of the cytoplasm and nucleus, chromatin
condensation and fragmentation, cytoskeletal collapse, membrane
blebbing, and finally, disintegration of the cell into apoptotic
bodies, which are engulfed by adjacent cells, thereby avoiding an
inflammatory response. It serves to model tissues during embryonic
development, to regulate cell number by eliminating excess cells, and
to remove damaged, mutated or infected cells. Defective or excessive
apoptosis can lead to cancer or autoimmune and degenerative diseases,
respectively. Apoptosis is executed by a family of cysteine proteases,
the caspases, which function in a proteolytic cascade that is
initiated by either the intrinsic mitochondrial-based pathway leading
to apoptosome formation, or the extrinsic pathway, which involves
activation of death receptors by their extracellular ligands to form
the DISC. The most distal caspases, known as the executioner caspases,
cleave numerous cellular substrates, thereby leading to specific
dismantling of the cell. Apoptosis is regulated by multiple proteins
at several levels, including the Bcl-2 family, which regulate the
release of apoptogenic factors from the mitochondria, and the IAP
family, which regulate caspase activity, and is countered by survival
signals eminating from the NF-kB signaling pathway. Although most of
the regulation occurs at the post-translational level, involving
protein-protein interactions, proteolysis, changes in subcellular
localization and phosphorylation, transcriptional control, such as by
p53, can also modulate the expression levels of several key apoptotic
proteins.
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
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In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.
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To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1107050000 | BioModels
Project description:The immunosuppressive tumor microenvironment (TME) remains a major obstacle to tumor control and causes suboptimal responses to immune checkpoint blockade (ICB) therapy. Thus, developing feasible therapeutic strategies that trigger inflammatory responses in the TME could improve the ICB efficacy. Mitochondria play an essential role in inflammation regulation and tumor immunogenicity induction. Herein, we report the discovery and characterization of a new class of previously unappreciated small molecules that can recapitulate aqueous self-assembly behavior, specifically target cellular organelles (e.g., mitochondria), and invigorate tumor cell immunogenicity. Mechanistically, this nanoassembly platform dynamically rewires mitochondria, induces endoplasmic reticulum stress, and causes apoptosis/paraptosis-associated immunogenic cell death. After treatment, stressed and dying tumor cells can act as prophylactic or therapeutic cancer vaccines. In preclinical mouse models of cancers with intrinsic or acquired resistance to programmed death-1 (PD-1) blockade, the local administration of nanoassemblies inflames the immunologically silent TME and synergizes with ICB therapy, generating potent antitumor immunity. This chemically programmed small-molecule immune enhancer acts like no other reported cytotoxic therapeutics and offers a promising new strategy for synchronous and dynamic tailoring of innate immunity to achieve traceless cancer therapy and overcome immunosuppression in cancers.
2024-08-01 | GSE272255 | GEO
Project description:The function of DFNA5 remained unknown for a long time, but previous functional studies by Op de Beeck et al. (2011) revealed that DFNA5 induces a growth defect in mutDFNA5- transfected HEK293T cells, as well as other cells, leading to PCD (Op de Beeck et al., 2011). The cell death-inducing capacity of DFNA5 was not only restricted to human cell lines, but was also observed in the yeast model Saccharomyces cerevisiae (Van Rossom et al., 2012). This inspired us to perform a transcriptomic analysis using two different model organisms (mammalian, HEK293T, and yeast, S.cerevisiae) to further elucidate the mechanisms related to DFNA5. Comparison of two HEK293T transfected cell populations, either with a WT or mutated DFNA5 gene. There are 5 biol reps for the WT transfected cells and 6 biol reps for the mut DFNA5 transfected cells.
2015-06-24 | E-GEOD-70167 | biostudies-arrayexpress
Project description:The function of DFNA5 remained unknown for a long time, but previous functional studies by Op de Beeck et al. (2011) revealed that DFNA5 induces a growth defect in mutDFNA5- transfected HEK293T cells, as well as other cells, leading to PCD (Op de Beeck et al., 2011). The cell death-inducing capacity of DFNA5 was not only restricted to human cell lines, but was also observed in the yeast model Saccharomyces cerevisiae (Van Rossom et al., 2012). This inspired us to perform a transcriptomic analysis using two different model organisms (mammalian, HEK293T, and yeast, S.cerevisiae) to further elucidate the mechanisms related to DFNA5.
2015-06-24 | GSE70168 | GEO
Project description:The function of DFNA5 remained unknown for a long time, but previous functional studies by Op de Beeck et al. (2011) revealed that DFNA5 induces a growth defect in mutDFNA5- transfected HEK293T cells, as well as other cells, leading to PCD (Op de Beeck et al., 2011). The cell death-inducing capacity of DFNA5 was not only restricted to human cell lines, but was also observed in the yeast model Saccharomyces cerevisiae (Van Rossom et al., 2012). This inspired us to perform a transcriptomic analysis using two different model organisms (mammalian, HEK293T, and yeast, S.cerevisiae) to further elucidate the mechanisms related to DFNA5.
2015-06-24 | GSE70167 | GEO